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Path - HANIN > immuno > Flashcards

immuno Flashcards

1
Q

Important gene in DiGeorges syndrome?

A

TBX1 gene

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2
Q

DiGeorge syndrome is also known as….

A

22q11.2 microdeletion

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3
Q

What pathogens do NK cells attack?

A

Intracellular pathogens (via downregulation of HLA-1 proteins on the surface)

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4
Q

Types of secondary immunodeficiencies

A

Malignancy - leukemia, lymphoma, myeloma
Drugs - steriods, cytotoxic drugs and immunosuppresants
Infection - HIV, measles, mycobacteria
Biochemical disorders - chronic renal failure, malnutrition

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5
Q

Hx of immunodeficiency

A 
Family histroy 
Chronic diarrhoea 
Recurrent infections 
Failure to thrive 
Mouth ulcers 
Skin rashes
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6
Q

What kind of infections do patients with IgA deficiency get?

A

Resp and GI infections

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7
Q

Who is at risk of getting IgA deficiency ?

A

Burns patients

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8
Q

What is PRR and what does it detect?

A

Innate immune system - Pathogen recognition receptors

Detects PAMPs

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9
Q

What can cells of the innate immune system secrete to help them regulate their immuneresponse?

A

Chemokines

Cytokines

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10
Q

Which cells are polymorphonuclear cells?

A

Basophils
Eosinophils
Neutrophils

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11
Q

Where are polymorphonuclear cells made?

A

Bone marrow

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12
Q

Role of polymorphonuclear cells?

A

Phagocytosis
Oxidative and non-oxidative killing
Release enzymes into granules
Express PRR and secrete cytokines and chemokines

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13
Q

What does infection cause the endothelium to do?

A

Expression adhesion molecules

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14
Q

What happens if there is a deficiency in macrophages

A

Recurrent infections in mouth and skin

Deep infections

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15
Q

What is an opsonins?

A

Coats pathogen to help with its recognition and clearance

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16
Q

Why does phagocytosis kill neutrophils?

A

Depletes them of their glycogen reserves and leads to apoptosis

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17
Q

What is oxidative killing?

A

NADPH oxidase complex converts oxygen into a reactive oxygen species - superoxide and hydrogen peroxide

Myeloperoxidase catalyses production of hydrochlorous acid from hydrogen peroxide and chloride;
hydrochlorous acid is a highly effective oxidant and anti-microbia

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18
Q

What is non-oxidative killing?

A

Use of bactericidal enzymes - lysozyme and lactoferrin into the phagolysome

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19
Q

What are the primary defects of phagocytes in primary immunodecifiency? More deets on next cards

A
  1. Issues to produce neutrophils
  2. Issues with migration of neutrophils
  3. Issues with endocytosis (eating) of pathogens
  4. Issues with formation of the phagolysome
  5. Issues with killing - oxidative and non-oxidative
  6. Issues with recruiting other cells during the killing process
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20
Q

What conditions lead to issues with recruitment (producing neutrophils)?

A
  • Reticular dysgenesis - failure of stems to differentiate along myeloid or lymphoid lineage due to mitochondrial mutation
  • Kostmann’s syndrome - autosomal recessive congenital condition which leads to severe neutropenia
  • Cyclic neutropenia - autosomal dominant condition leading to episodes of neutropenia every 4-6 weeks due to defect in ELA-2 (neutrophil elastase)
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21
Q

What conditions leads to issues with migration of neutrophils?

A
  • Leukocyte adhesion deficiency: due to issue with CD18 receptor usually found on the neutrophil surface. CD18 is used to bind to the surface of endothelium cells to regulate neutrophil adhesion. If this fails, neutrophils stay in the blood and can’t enter tissue

Patients tend to have a high neutrophil count but no abscess or pus formation

think LAD 18

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22
Q

What conditions leads to issues with endocytosis and formation of the phagolysosome?

A

Issues with complement or antibody formation will compromise opsonisation so making it harder to eat the pathogen

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23
Q

What condition leads to issues with killing - oxidative and non-oxidative?

A

Chronic granulatamous disease - failure of oxidative killing due to mutation of NADPH oxidase complex so it cant make reactive oxygen species/oxygen free radicals. Failure to breakdown intracellular pathogen

Patient will have constant inflammation, formation of granulomas, lymphadenopathy and hepatosplenomegaly

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24
Q

How to Ix chronic granulatamous disease?

A

Nitroblue tetrazolium test - which is supposed to change from yellow to blue in the presense of hydrogen peroxide

Dihydro-rhodamine (DHR) flow cytometry test

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25
Q

What conditions leads to issues with recruitment of other cells of the immune system?

A

Issue with IFN-gamma and IL-12. Infection with MYCOBACTERIA causes IL-12 to induce T-cells to produce IFN-gamma. This stimulates macrophages and neutrophils and stimualtes oxidative pathways

Patients with this condition are suspectible to mycobacteria infection

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26
Q

What kind of infections would we worry about in NK cell deficiency?

A

Viral infections especially herpes virus

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27
Q

What types of NK cell deficiency are there?

A

Classical - lack of NK cells (GATA2 and MCM4)

Functional - abnormal functioning NK cells (FCGR3A gene)

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28
Q

Tx of NK cell deficiency

A

Prophylaxis with aciclovir, gangclovir
Cytokines with INF-alpha can be used to stimulate NK cells cytotoxicity
Haematopoietic stem cell transplantation

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29
Q

Where is complement made?

A

Liver

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30
Q

Different pathways involved with complement cascade

A

Classical : C1, C2, C4. Activated by antigen-antibody complexes
Alternative - directly triggered by C3 to bacterial cell wall
Mannon binding lectin - C2 and C4. Activates classical pathway

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31
Q

Whats the most important part of the complement cascade

A

C3 - amplication of the complement cascade and triggers the formation of the MAC (membrane attack complex) via C5-C9.

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32
Q

Which pathogens are people with a complement deficiency more at risk to?

A

Encapsulated organisms: N.mengitiditis, h.influenzae, s.pneumoniae

SLE patients are at risk if earlier components of complement cascade involved

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33
Q

Which complement deficiency is associated with SLE?

A

C2 and mainly the classical pathway complement proteins

Failure to clear necrotic cells - autoimmunity risk?

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34
Q

Mannan binding lectin pathway deficiency?

A

MBL deficiency is relatively common, with 10% having no MBL. It is associated with increased infection in patients with another cause of immune impairment, e.g.
premature infants, chemotherapy patients, HIV patients, and antibody deficiency
patients.

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35
Q

What happens if there are defects in the aternative pathway?

A

If there are defects in the alternative pathway, there is an inability to mobilise complement rapidly in response to bacterial infections, and there will be recurrent infection with encapsulated bacteria. It is very rare – factor B, I and P deficiency can all occur.

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36
Q

What is there is a C3 deficiency?

A

leads to severe susceptibility to infection from bacteria, and an increased risk of development of connective tissue disease. A defect in the terminal common pathway results in an inability to make membrane attack complexes or use complement to lyse encapsulated bacteria. It results in a very specific hole in the immune system, leading to opportunistic infections by Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae.

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37
Q

Cause of secondary complement deficiency?

A

Glomerulonephritis

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38
Q

Ix complement deficiency?

A

blood samples measuring C1 and C4

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39
Q

What do T-cells express on their surface?

A

CD3, CD4 or CD8

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40
Q

How do T-cells communicate with immune cells from the innate immune system?

A

APC via HLA molecule complex

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41
Q

CD4 has an affinity for which HLA complex?

A

HLA-II

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42
Q

CD8 has an affinity for which HLA complex?

A

HLA-I

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43
Q

Role of TH1

A

Helps CD8 T cells and macrophages

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44
Q

Role of TH17

A

Helps neutrophil recruitment

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45
Q

Role of Treg

A

IL-10/TGF beta expressing?

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46
Q

How is CD8 cytotoxic?

A

Perforin, granzymes and expression of FAS ligand which binds to fats and causes apoptosis

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47
Q

Patients with T-cell deficiency are more at risk of getting what kind of infections?

A

Viral infections - CMV
Some fungal
Some bacterial
Early malignancy

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48
Q

Patients with B-cell/antibody deficiency are more at risk of getting what kind of infections?

A

Bacterial infections
Toxins - diptheria
Some viral

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49
Q

Why do babies with SCID present after 3 months?

A

Maternal immunoglobulin protection (active transport of IgG across the placenta)

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50
Q

More on reticular dysgenesis

A

SCID
Failure to differentiate lymphoid and myeloid lineage so you dont make lymphocytes, macrophages, neutrophils and platelets
Mutation - in mitochondrial energy
metabolism enzyme Adenylate Kinase 2 (AK2)
Fatal unless haematopoetic stem cell transplantation

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51
Q

X-lined SCID

A

Mutation of the gamma chain of IL-2 receptor

Causes inability to respond to cytokines and produce mature B-cells

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52
Q

DiGeorge syndrome

A 
Mutation on chromosome 22 (22q11.2) 
Thymic hypoplasia 
Hypocalcemia 
B-cells normal 
T-cell reduced
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53
Q

Bare lymphocyte syndrome

A

This is a defect in one of the regulatory proteins
involved in Class II gene expression, typically regulatory factor X or Class II Transactivator.

There is an absent expression of MHC Class II molecules, leading to a profound deficiency of CD4+ cells, but a normal number of CD8+ cells.

There will be a normal number of B cells, but a failure to make IgG or IgA antibodies. BLS I also exists, which is a failure to express HLA Class I. These children normally become unwell at 3 months, with infections of all types and failure to thrive.

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54
Q

Cytokine deficiencies

A

IL-12 and IFN-gamma = mycobacterial infection susceptiblity

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55
Q

Risk of IL12 and IFN-gamma deficiency

A

Mycoplasma infection
Infection after BCG vaccine
Salmonella
Unable to form granulomas

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56
Q

Bruton’s Agammaglobulinaemia

A

X-linked tyrosine kinase defect
BTK gene mutation
Issue making mature B-cells
Symptoms occur 3-6 months of age due to maternal protection

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57
Q

HyperIgM syndrome

A

X-linked - Xq26
Failure of isotype switching
Detective CD40L gene , DC154
Basically means that activated T-cells cant chat to B-cells about what antibodies they need to make
elevated serum IgM, and undetectable IgA, IgE, IgG

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58
Q

Common variable immune deficiency

A

This presents with recurrent bacterial infections (often with severe end-organ damage), autoimmune disease, and granulomatous disease, as a result of low IgG, IgA, and IgE. The cause is unknown. It is a heterogenous group of disorders

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59
Q

Symptoms of IgE hypersensitivity

A

angioedema,urticaria, pruritus, rhinitis conjunctivitis,

wheeze, diarrhoea, vomiting, and anaphylaxis

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60
Q

How long before skin prick test do you discontinue antihistamines?

A

48 hours

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61
Q

How do you investigate allergy?

A

Skin prick test (+ >2mm wheal)
Challenge test
During an acute episode - look for mast cell degranulation via mast cell tryptase levels (peak - 1 hr)
Component resolved diagnositics
Quantitative specific IgE to putative allergen (RAST)

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62
Q

What is component resolved diagnostics?

A

Measures IgE response to specific allergen protein

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63
Q

CRD - if patient is allergic to peanuts, what allergen protein is it?

A

Ara h2

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64
Q

What is the challenge test?

A

So you supervise them while they eat and see what happens (double blind - gold standard)
Risk of severe reaction

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65
Q

Define anaphylaxis

A 
Severe hypotension 
Laryngeal oedema 
Difficulty breathing 
Angioedema 
Utricia
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66
Q

During anaphylaxis, when do you measure serum typtase levels?

A

1 hour, 3 hours and 24 hours

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67
Q

Mx of anaphylaxis

A 
IM adrenaline 500 mcg 
Oxygen 
Inhaled bronchodilators 
IV hydrocortisone 100mg 
IV fluids
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68
Q

How much adrenaline is in an epipen?

A

300mcg for adults

150mcg for kids

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69
Q

Symptoms of allergic rhinitis

A

Nasal discharge, sneezing, loss of smell, nasal obstruction and itchiness, eye symptoms

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70
Q

What triggers allergic rhinitis?

A

Pets
Plants
Latex

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71
Q

Tx of allergic rhinitis

A

Oral histamines
Nasal corticosteriod spray
Monteleukast

72
Q

Which cytokines are involved in allergy?

A

IL4, IL5, IL-10 (TH2)

73
Q

Type 2 hypersensitivity?

A

IgM or IgG reacts with self-antigens. Usually of a specific tissue rather than systemic (antibody-mediated)

  • Complement activation
74
Q

How can you test for Type 2 hypersensitivity?

A

DAT (coombs) test

75
Q

Examples of conditions which are type-2 hypersensitivity mediated?

A 
Grave's disease 
Haemolytic disease of the newborn
Autoimmune haemolytic anaemia 
Goodpastures 
Mysathenia Gravis 
Wegener's granulomatosis
76
Q

What is type III hypersensitivity?

A

Antibody-antigen complexes deposit in blood vessel walls and cause inflammation and damage

77
Q

Difference between type II and type III hypersensitivity?

A

Complement activation is much greater in type III
Type II - antigen is not soluble whereas type III it is
Type II - more specific to tissue
Type III - more systemic

78
Q

Examples of type III hypersensitivity reactions

A

SLE
Serum sickness
Polyarteritis nodosa - hep B
Mixed essential cryoglobulinaemia - assoc. hep c

79
Q

What is type IV hypersensitivity?

A

T-cell mediated

80
Q

Examples of type IV hypersensitivity?

A 
Contact dermatitis 
Mantoux test 
RA
IBD 
MS 
TIDM + hashimotos (CD8)
81
Q

HLA association for RA?

A

HLA DR4

82
Q

HLA association for Ankylosing spondylitis?

A

HLA B27

83
Q

HLA association for Goodpastures syndrome

A

HLA DR15 / DR2

84
Q

HLA association for SLE

A

HLA DR3

85
Q

HLA association for T1DM

A

HLA DR 3/4

86
Q

HLA assocation for grave’s disease

A

HLA DR3

87
Q

Who is more likely to get sjorgen syndrome

A

Women

88
Q

What is sjorgens syndrome?

A

Autoantibodies against the exocrine glands (tear and salivary glands)

89
Q

Which antibodies are seen in sjorgens syndrome?

A

ANA +
Anti-Rho
Anti-La

90
Q

Symptoms of sjorgen syndrome

A

Dryness of body surfaces
Keratoconjuctivitis - red, itchy eye with blurred vision
Ulceration and perforation of the nasal sputum
Infection prone

91
Q

IPEX?

A

IPEX (immunodysregulation polyendocrinopathy enteropathy X-linked syndrome) is a rare disease linked to the dysfunction of the transcription factor FOXP3, widely considered to be the master regulator of the regulatory T cell lineage.

92
Q

What HLA is associated with coeliac disease?

A

HLA-DQ2 or HLA-DQ8 (To eat or not to eight)

93
Q

What antibodies are there in coeliac disease?

A

Anti-tissue transglutaminase antibody
Anti-endomysial antibody
Anti-Gliadin antibody

94
Q

What do you see in coeliac disease histopathology?

A

Crypt hyperplasia
Villous atrophy
Lymphocyte infiltration

95
Q

What skin manifestation is associated with coeliac disease?

A

Dermatitis herpetiformis

96
Q

How can you boost the immune system?

A

Vaccination
Human normal immunoglobulin
Specific immunoglobulin (post exposure prophylaxis)
Recombinant cytokines

97
Q

What kind of antibody class does Human normal immunoglobulin contain?

A

IgG against full range of organisms

98
Q

Who receives human normal immunoglobulin?

A

Primary immunodeficiency where they cant make antibodies: SCID, Bruton’s agammaglobulinaemia, CVID,

Secondary immunodeficiency where they cant make antibodies anymore : malignancy, bone marrow suppression

99
Q

What conditions can you get post exposure prophylaxis

A

Hepatitis B
Tetanus
Rabies
Varicella zoster

100
Q

What kind of recombinant cytokines do you give and to who?

A

Interferon-alpha: hep b, hep c, kaposi sarcoma, CML, hairy cell leukemia
Interferon-beta - relapsing MS
Interferon-gamma - chronic granulomatous disease

101
Q

co-stimulation for T-cell activation

A

CD28 and B7

102
Q

How does Ipilimumab work?

A

Stops the upregulation of CTLA-4 which stops the activation of T-cells so you get more T-cells

103
Q

Who do we give Ipilimumab to?

A

Advanced melanoma

104
Q

How does Pembrolizumab work?

A

specific to PD-1 and so stops upregulation and allows T-cells activation

105
Q

How do we suppress the immune system?

A
  • Non-specific immunosuppresion
  • Remove the antibodies
  • Target specific components of the immune response
106
Q

What cytokine is involved with T-cell proliferation?

A

IL-2

107
Q

How can we suppress T-cells before they meet APCs?

A

Anti-T-cell monoclonal antibodies

108
Q

How do we suppress the proliferation of T-cells?

A

Corticosteriods

Inhibitors of cell signalling

109
Q

How do we suppress the effector function of T-cells?

A

Plasmapheresis
Corticosteriods
Anti-IL-12/IL-23 monoclonal antibody

110
Q

Symptoms of an infusion reaction?

A

Ig-E type I hypersensitivity reaction

Wheeze, hypotension, urticaria, headaches, fevers and myalgia

111
Q

Why are corticosteriods immunosuppressive?

A

Inhibits phopholipase A2 and so inhibits arachidonic acid. Reduces prostagladin synthesis and so inhibits phagocytosis, expression of adhesion molecules
Increases apoptosis of lymphocytes
Decreases antibody production

112
Q

How do cytotoxic drugs cause immunosuppresion

A

Inhibit DNA synthesis in rapidly dividing cells

113
Q

Different types of cytotoxic drugs

A

Methotrexate
Azothioprine
Cyclophophamide
Mycophenolate

114
Q

When do we use methotrexate and how does it work?

A

Used in ectopic pregnancy
RA
Crohns
Psoriasis

Mechanism - antifolate cos inhibits dihydrofolate reductase so inhibits DNA synthesis

115
Q

When do we use aziothioprine and how does it work?

A

Used in autoimmune disease
Transplantation

Mechanism: anti-metabolite agent which stops the production of adenine and guanine. Metabolised in the liver to 6 mercaptopurine. Inhibits replication of DNA

116
Q

When do we use cyclophosphamide and how does it work?

A

Anti-cancer agent
Vasculitis
Connective tissue disease

Mechanism: affects b-cells more than t-cells. Damages DNA by alkylating guanine and prevent cell replication

117
Q

Who needs plasmapheresis?

A

Severe-antibody mediated disease like:

  • Goodpastures
  • Mysathenia

Antibody mediated rejection

118
Q

Risk of plasmapheresis

A

Anaphylaxis

119
Q

What drugs inhibit cell signalling?

A 
Tacrolimus - IL-2 inhibitor 
Sirolimus - blocks clonal proliferation of t-cells 
Cyclosporin - IL-2 inhibitor 
Tofactinib - JAK inhibitor 
Apremilast - PDE4 inhibitor
120
Q

What drugs are used in rejection prophylaxis in transplantation?

A

Tacrolimus and Cyclosporin

SE: nephrotoxic, hypertension, neurotoxic

121
Q

What agents are directed at cell-surface antigens for immunosuppression

A

Rituximab - anti-CD20 (depletes mature B cells)
Abatacept - anti-CTLA4 (reduces T-cell activation)
Basiliximab - anti-CD25 (related to alpha chain IL-2)
Natalizumab - anti-alpha 4 integrin
Tocilizumab - anti-IL-6
Daclizumab - anti-IL2

122
Q

Abatacept

A

Anti-CTLA4 (reduces T-cell activation)

123
Q

Basiliximab

A

Anti-CD25 (related to alpha chain IL2)

124
Q

Natalizumab

A

Anti-alpha 4 integrin (inhibits T-cell migration via VCAM1)

125
Q

Tocilizumab

A

Anti-IL6

126
Q

Daclizumab

A

Anti-IL2

127
Q

Infliximab

A

Anti-TNF alpha

128
Q

Golimumab

A

Anti-TNF alpha

129
Q

Entanercept

A

TNF alpha/TNF beta

130
Q

Denosumab

A

Anti-RANK ligand (bone SE) and used for bone malignany and osteoporosis

131
Q

Which chromosome encodes HLA complex

A

Chromosome 6

132
Q

Which HLA classes are on every cell?

A

HLA-CLASS I A, B, C,

133
Q

Which HLA classes are just on APCs but can be upregulated on other cells in times of stress?

A

HLA-class DP, DQ, DR

134
Q

When sel sel and her bestie got transplant, what was good about their HLAs?

A

Minimising HLA difference between donor and recipient improves transplant outcomes.

135
Q

What is hyperacute transplant rejection? (mins-hours)

A

When the recipient has preformed antibodies that activate complement cascade

Thrombosis and necrosis

Tx: prevent via ABO groups crossmatching and HLA matching

136
Q

What is acute-cellular transplant rejection? (weeks-mths)

A

CD4 activating a Type IV reaction

Tx: T-cell immunosuppression

137
Q

What is acute-antibody mediated transplant rejection? (weeks - mths)

A

B-cell activation producing antibodies

Tx: plasmapheresis and B-cell immunosuppression

138
Q

What is chronic transplant rejection? (mths-yrs)

A

Can be immune and non-immune

Risk factors:

  • High BP
  • Hyperlipidaemia
  • Multiple acute rejections

Path: fibrosis, vasculopathy, bronchiolitis

Tx: minimise organ damage

139
Q

GVHD (days-weeks)

A

Donor cells start fighting host

Symptoms: rash, D+V, bloody stool, jaundice

Tx: corticosteriods

140
Q

When selena and her bestie went to get matched, what happened?

A

You need to determine the donors and recipient blood group and HLA type via PCR. Make sure they are v.similar

Check that the donor doesnt already have pre-formed antibodies against the donors HLA or ABO group via complement dependent cytoxicity, flow cytometry etc

Cross match them to make sure they dont react

After the transplant, check for new antibodies

141
Q

How does haematopoietic stem cell transplant work?

A
  • Eliminate hosts immune system via total body irradiation or cyclophophamide
  • Replace with new bone marrow
142
Q

What are post-transplant complications?

A
  • immunosuppressed so more likely to get oppurtunistic infections
  • Increased risk of malignancy - esp viral associated such as EBV (lymphoproliferative disease), HHV8 (kaposi sarcoma)
  • Atherosclerosis
143
Q

Isograft

A

Transplant from twin

144
Q

Allograft

A

from same species (human)

145
Q

Xenograft

A

from different species

146
Q

Split graft

A

shared by two recipients

147
Q

How does HIV bind to CD4 cells?

A

GP120 + GP41 and co-receptor CCR5 + CXCR4

148
Q

What type of virus is HIV?

A

single stranded RNA retrovirus

149
Q

What enzyme does HIV use?

A

reverse transcriptase (converts RNA –> DNA)

150
Q

How does HIV affect CD8 T-cells?

A
  • Infected CD4+ T cells are also anergised by the virus,
    meaning CD8+ cellscannot be primed, and CD4+ and CD8+ responses are greatly diminished
  • Infected macrophages and dendritic cells are killed by the virus, leading to defects in antigen presentation, and failure to activate memory responses.
151
Q

Steps in viral replication

A 
Attachment/Entry 
Reverse transcription and DNA synthesis 
Integration 
Viral transcripton
Viral protein synthesis 
Assembly of virus and release of virus 
Maturation
152
Q

What is the innate immune response to HIV?

A

Non-specific activation of macrophages, NK cells and complement

Stimulation of dendritic cells via TLR

Release of cytokine and chemokines

153
Q

What is the adaptive response to HIV?

A

Neutralising antibodies: Anti-GP120 and anti-GP41
Non-neutralising antibodies: anti-pg24 gag IgG
CD8 tcells secrete chemokines MIP-1a, 1b and RANTES

154
Q

How does HIV damage the immune system?

A
  • HIV remains infectious even when Ab coated

 Activated infected CD4+ helper T cells are killed by CD8+ T cells

 Activated infected CD4+ helper T cells are anergised (disabled)

 CD4 T-cell memory lost & failure to activate memory CTL

 Monocytes and dendritic cells are therefore not activated by the CD4+ T cells and cannot prime naïve CD8+ CTL (due to impaired antigen presenting functions)

 Infected monocytes and dendritic cells are killed by virus or CTL

 Quasispecies are produced due to error-prone reverse transcriptase = these escape from immune response

 Effective immunity requires antibodies to prevent infection and neutralize virus, and sufficient CTL to eliminate latently infected cells

155
Q

Shit i think i have HIV, how do i get diagnosed?

A

Screening : anti-HIV ab via ELISA

Confirmation: Western blot detects ab

This must be done 10 weeks post exposure due to seroconversion

156
Q

How are HIV patients monitored?

A

Viral load - via PCR
CD4 count - via flow cytometry
AIDs - less than 200 CD4 count

157
Q

Tx of HIV

A

HAART

Pregnancy- Zidovudine (oral during pregnancy, IV during labour) and give to baby for 6 weeks

158
Q

Vaccination schedule

A

https://memorize.com/uk-vaccination-schedule/michaelokocha

159
Q

Memory T-cells

A

CD45 RO

160
Q

Naive T-cells

A

CD45 RA

161
Q

Where are central memory cells found (CCR7+)

A

Lymph nodes and tonsils

162
Q

What do central memory cells produce

A

IL-2

163
Q

Where are effector memory cells found (CCR7-)

A

Liver, lungs and gut

164
Q

What do effector memory cells produce

A

INF-gamma and perforin

165
Q

CCR7?

A
  • CCR7 binds CCL19 and CCL21 present on the luminal surface of endothelial cells in lymph nodes which causes firm arrest and the initiation of extravasation.
     CCR7 directs homing of dendritic cells to lymph nodes
     CD62L interacts with a molecule on HEV, which mediates attachment and rolling
166
Q

B-cell memory

A

B cells stimulated by antigen -> expansion/isotope switching (due to cytokines provided by T helper cells) -> plasma cells producing antibody/memory cells

 Memory cells that can differentiate into plasma cells (long lived)

 These cells produce: Quicker response, more antibodies, higher affinity antibodies,
more IgG and generally better antibodies.

167
Q

TH1

A

IL-12, IFN-gama and TNF

168
Q

TH2

A

IL-4, 5, 6

169
Q

Which cytokine is the first to be released during initial exposure to the allergen

A

IL-12

170
Q

CH50 and AP50 tests

A

complement deficiencies

171
Q

Tx for wegener’s g

A

Corticosteroids,
cyclophosphamide
co-trimoxazole

172
Q

Tx for chaug-strauss syndrome

A

Prednisolone,
Azathioprine,
Cyclophosphamide

173
Q

Tx for goodpastures and pemphigus valigarus

A

Corticosteroids and immunosuppression

174
Q

Mixed Essential Cryoglobulinaemia

A

Associated with Hep C antigens - IgM and IgG

175
Q

↓C4

A

SLE

176
Q

Tx of MS

A

Corticosteroids,

Interferon-β

Path - HANIN (5 decks)

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